H yponatremia in exercise is a potentially dangerous clinical scenario previously thought to be limited to exercise bouts of long duration and associated with excessive water intake. We report the case of a healthy young athlete with hyponatremia after moderate-duration exercise and only moderate water intake. CASE REPORTA 19-year-old female novice triathlete presented with abrupt onset of dull, bioccipital headache associated with mild photophobia; nausea with clear, watery emesis; and generalized malaise 90 minutes after completing a sprint distance event (0.4-km swim, 17-km bike, and 5-km run) in 1 hour 33 minutes. The outdoor ambient temperature at the race's completion at approximately 9 AM was 32°C. She reported hydration with 3 L of water the evening before the race, approximately 500 mL during the race, and 700 mL after the race. Her food intake was minimal on the morning of the race.Although she was an inexperienced triathlete, she was physically fit (weight, 57 kg; height, 160 cm; body mass index, 22 kg/m 2 ) and finished the race first among female novices. The patient's medical history included exercise-induced bronchospasm and a seizure disorder that had been asymptomatic for years. For seizure prophylaxis, she was taking carbamazepine and lamotrigine, tapering down her carbamazepine while increasing her lamotrigine. Serum levels of carbamazepine and sodium drawn 3 days before the race were 5.7 mg/mL (therapeutic range, 4-10 mg/mL) and 142 mmol/L, respectively.Physical examination revealed an oral temperature 36.1°C, heart rate of 70 beats/min, blood pressure of 128/82 mm Hg without orthostatic change, and respiratory rate of 12 breaths/min. She was alert and oriented, with equal and reactive pupils, intact extraocular motion, and a noticeable tearing mechanism. Her oral mucus membranes were moist, her skin was cool and moist, and she had no detectable edema. Findings on cardiac, pulmonary, abdominal, and neurologic examinations were all normal, as was her mental status. Possible hyponatremia was diagnosed, and she was transported to a local emergency department for further evaluation and management.Laboratory studies in the emergency department confirmed the diagnosis: sodium, 127 mmol/L; potassium, 3.5 mmol/L; chloride, 97 mmol/L; bicarbonate, 21 mmol/L; glucose, 4.8 mmol/L; creatinine, 88.4 mmol/L; urea nitrogen, 3.6 mmol/L; and serum osmolality, 254 mOsm/kg.

The novel Sars-CoV-2 virus causes a viral pneumonia (COVID-19) and corticosteroids have been shown to prolong viral shedding and may increase mortality in viral pneumonias(1). Patients with asthma typically require inhaled corticosteroids. It is unknown if asthmatics will therefore have worse outcomes as a result. METHODS: This is a retrospective cohort study of asthmatics compared to the general population diagnosed with COVID-19 pneumonia from a multicenter health system in Kansas City. The primary outcome is admission to a hospital. Secondary outcomes include mechanical ventilatory support and in-hospital all-cause mortality. RESULTS: In this cohort, asthmatics had an average BMI of 32.9 +-3.2, as compared to 31.2+-0.8 in the general population. Mean age is 49.0 +-6.0 vs 54+-1.79. As of 5/1/2020 there have been 345 patients positive for COVID 19. 24 have asthma. 7/24 with asthma (29.2%) vs 79/321 non-asthmatics (24.6%, OR 1.26, p¼0.6) have required admission to a hospital. 2/24 (8.3%) asthmatics have required mechanical ventilation vs 17/321 (5.2%, OR 1.49, p¼0.6) non-asthmatics. 0 asthmatics have died and 7/ 321 (2.8%, OR 0.8, p¼0.9) non-asthmatics have died. CONCLUSIONS: In conclusion, based on this limited retrospective data, asthma does not appear to be a significant risk factor for hospital admission, mechanical ventilation, or death. CLINICAL IMPLICATIONS: Larger, prospective studies are needed to ensure asthmatics are not at increased risk of worse outcomes due to COVID-19.

A patient with a history of Crohn's disease on infliximab presented to the hospital with sepsis and a new heart murmur. He was found to have native aortic valve infective endocarditis from a rare species of group D Streptococcus in his blood. The patient was also noted to be in an acute flare of Crohn's disease. The hospital course was complicated by florid heart failure from acute aortic insufficiency. He eventually improved after source control and appropriate antibiotic therapy. S. pasteuranis bacteremia and endocarditis are attributable to the patient's immunocompromised state as a result of infliximab treatment. While S. pasteuranis is infrequently grown in blood cultures, it is commonly found in normal gut flora. We hypothesize that it gained access to the bloodstream through the epithelium in the terminal ileum, which was inflamed due to an acute flare of Crohn's disease.

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